Vascular Depression Research Articles

Do supportive work environments matter for minority aging? Work stress and subjective cognitive impairment among middle-age and older lesbian, gay, bisexual, transgender, and queer adults

Research has documented how people's experiences at work affect their cognitive health outcomes, but how these processes unfold for minority groups, particularly lesbian, gay, bisexual, transgender, and queer (LGBTQ+) populations, is unclear. This study builds on the nascent literature by employing generalized structural equation models to test how experiencing major problems at work and working with LGBTQ+ supportive coworkers affect subjective cognitive impairment among middle-age and older LGBTQ+ adults. We also test for mediated and indirect effects of support and problems at work operating via vascular disease, sleep problems, and depression symptoms. Experiencing major problems at work is associated with a higher likelihood of reporting cognitive symptoms consistent with mild cognitive impairment, but this relationship is mediated by depression symptoms and sleep problems. Having LGBTQ+ supportive coworkers does not have direct effects on mild cognitive impairment, but does operate indirectly by decreasing problems at work and, in turn, decreases the likelihood of reporting cognitive symptoms consistent with mild cognitive impairment. Overall, we find that workplace stressors contribute to cognitive health directly and through mediated and indirect pathways and that supportive contexts reduce exposure to problems at work. We conclude with suggested possibilities to reorganize workplaces to improve long-term cognitive health outcomes for older adults, especially those who are LGBTQ+-identified.

Depression in patients with cerebral microangiopathy

Cerebral microangiopathy (CMA) is one of the significant causes of depression in the elderly. Close associations of the risk of developing depression with white matter hyperintensity, the presence of lacunar infarcts, and other markers of vascular disease are shown. The available data suggest that various vascular mechanisms, in particular, involvement of small vessels of the brain, generalized microvascular and endothelial dysfunction, metabolic risk factors, – are risk factors for the development of depression. Pathogenetic mechanisms include cerebral hypoperfusion and immune dysregulation. Depression is also a common complication of coronavirus infection, occurring both in the acute and postCOVID periods. The same mechanisms as in vascular depression are involved in the pathogenesis of the development of post-COVID depressive disorders. Given the complexity of the mechanisms of development of depressive disorders in patients with CMA, the presence of severe comorbid vascular pathology, antidepressants with an optimal ratio of efficacy and safety should be preferred. Agomelatine (Valdoxan) is one of such drugs.

Association between vascular access type and depression in hemodialysis patients.

Hemodialysis is the most common treatment used for end-stage kidney disease (ESKD) patients and an arteriovenous fistula (AV) fistula is the preferred vascular access. The goal of our study was to investigate potential associations between vascular access type and depression. This was a cross-sectional survey of 180 patients receiving maintenance hemodialysis. The Beck Depression Inventory was used to assess degree of depression. Demographic factors, treatment details, and laboratory values were obtained from the hospital medical record. Fifty-two percent (n = 93) of the patients were being dialyzed using an AV fistula and 48% (n = 87) via a tunneled cuffed catheter. No significant differences were found between access type use in terms of gender (p = 0.266), presence of diabetes, hypertension, or peripheral artery disease (p = 0.409, p = 0.323, p = 0.317; respectively). The prevalence of Beck Depression Inventory scores greater than 14 (marking presence of depression) was significantly higher in the patients being dialyzed with a tunneled cuffed catheters (61%) compared to patients dialyzed with an AV fistula (36%) (p = 0.001). We found statistically higher depression scores among patients receiving hemodialysis with a tunneled cuffed catheter.

Association of Alzheimer’s Plasma Biomarker Concentrations with Body Mass Index in Older Adults (P10-6.005)

<h3>Objective:</h3> To evaluate the relationship of chronic medical conditions and other characteristics, including body mass index (BMI), vascular risk factors, depression, head injury and education, with cognitive impairment and blood-based biomarkers of Alzheimer’s pathology, phosphorylated tau (P-tau 181, P-tau 217), in a multi-ethnic cohort. <h3>Background:</h3> Studies suggest that comorbidities may influence the levels of blood-based biomarkers for Alzheimer’s disease and their interpretation; however, these relationships must be further explored in ethnically diverse cohorts. In our recent multi-ethnic cohort study, 47% of cognitively impaired participants had low P-tau concentrations, and 31% of unimpaired participants had high P-tau concentrations. We sought to determine whether differences in risk factor profiles may help to explain the discordant groups in the same cohort. <h3>Design/Methods:</h3> Three hundred participants aged 65 and older were selected from a prospective community-based cohort for equal representation among three racial/ethnic groups: non-Hispanic White, Hispanic/Latino and African American/Black. Participants were classified into four diagnostic groups based on absence (Asym)/presence (Sym) of cognitive symptoms and low(−)/high(+) P-tau, determined in the same cohort: (Asym/P-tau−, Asym/P-tau+, Sym/P-tau−, Sym/P-tau). We examined differences in participant characteristics across the four groups. For significant factors, we also examined two-group differences according to cognitive symptoms (Asym/Sym) and P-tau (P-tau+/P-tau−). <h3>Results:</h3> BMI was lower in individuals with high P-tau 217 and 181 concentrations (25.7 vs. 27.9 kg/m²; 25.3 vs. 27.9 kg/m², respectively) but did not differ across dementia groups. Education was lower in individuals with dementia compared to those without (9.1 vs. 12.5 years), and it did not vary according to P-tau level. Frequencies of hypertension, diabetes, heart disease, smoking, head injury and depression did not differ between the four groups. <h3>Conclusions:</h3> Lower BMI is associated with higher P-tau concentrations but not with the presence or absence of dementia. This finding suggests that Alzheimer’s pathology may be accompanied by metabolic changes regardless of cognitive status. <b>Disclosure:</b> Ms. Hoost has nothing to disclose. Adam Brickman, PhD has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Cognition Therapeutics. Annie Lee has nothing to disclose. The institution of Dr. Gu has received research support from NIH. Ms. Sanchez has nothing to disclose. Mrs. Reyes-Dumeyer has nothing to disclose. Dr. Honig has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Eisai. Dr. Honig has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Biogen. Dr. Honig has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Medscape. Dr. Honig has received personal compensation in the range of $5,000-$9,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Prevail. Dr. Honig has received personal compensation in the range of $10,000-$49,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Cortexyme. Dr. Honig has received personal compensation in the range of $10,000-$49,999 for serving as an Expert Witness for Legal Firms . The institution of Dr. Honig has received research support from Roche. The institution of Dr. Honig has received research support from Eisau. Dr. Honig has received research support from Alector. The institution of Dr. Honig has received research support from Transposon. The institution of Dr. Manly has received research support from NIH. Dr. Manly has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant with University of Mississippi. Rafael Lantigua has nothing to disclose. Dr. Kang has nothing to disclose. Dr. Dage has received personal compensation for serving as an employee of Eli Lilly and Company. Dr. Dage has stock in Eli Lilly and Company. Dr. Dage has stock in General Electric. Dr. Dage has received research support from Indiana University School Of Medicine. Dr. Dage has received intellectual property interests from a discovery or technology relating to health care. Dr. Mayeux has nothing to disclose.

Positive airway pressure therapy for post-stroke sleep disordered breathing: a systematic review, meta-analysis and meta-regression.

Sleep disordered breathing (SDB) is an under-recognised independent risk factor and a potential consequence of stroke. We systematically reviewed and meta-analysed the effectiveness of positive airway pressure (PAP) therapy in improving post-stroke outcomes. We searched CENTRAL, Embase, PubMed, CINAHL, PsycINFO, Scopus, ProQuest, Web of Science and CNKI (China National Knowledge Infrastructure) for randomised controlled trials comparing PAP therapy against a control or placebo group. We evaluated the pooled effects of PAP therapy on recurrent vascular events, neurological deficit, cognition, functional independence, daytime sleepiness and depression using random effects meta-analyses. We identified 24 studies. Our meta-analyses showed that PAP therapy reduced recurrent vascular events (risk ratio 0.47, 95% CI 0.28-0.78), and showed significant beneficial effects on neurological deficit (Hedges' g= -0.79, 95% CI -1.19- -0.39), cognition (g=0.85, 95% CI 0.04-1.65), functional independence (g=0.45, 95% CI 0.01-0.88) and daytime sleepiness (g= -0.96, 95% CI -1.56- -0.37). However, there was insignificant reduction in depression (g= -0.56, 95% CI -2.15-1.02). No publication bias was detected. Post-stroke patients with SDB benefited from PAP therapy. Prospective trials are needed to determine the ideal initiation period and the minimum effective therapeutic dose.

Elevated frequency and everyday functioning implications of vascular depression in persons with HIV disease

Depression and cardiovascular disease are common and associated with one another in HIV disease. This study aimed to determine the frequency and everyday functioning implications of the clinical syndrome of vascular depression among people living with HIV (PLWH). Participants in this cross-sectional study included 536 PLWH and 272 seronegative individuals who completed a biomedical and psychiatric research evaluation. Vascular depression was operationalized as the current presence of: 1) two or more vascular conditions; and 2) depression as determined by a normative elevation on the Depression/Dejection subscale of the Profile of Mood States or a diagnosis of Major Depressive Disorder per the Composite International Diagnostic Interview. Everyday functioning was measured by both self- and clinician-rated activities of daily living. A logistic regression model showed that HIV was associated with a three-fold increased risk of vascular depression, independent of potential confounding factors. A second logistic regression model within the PLWH sample showed that PLWH with vascular depression had significantly greater odds of dependence in everyday functioning as compared to PLWH with either vascular disease or depression alone. The elevated frequency of vascular depression in PLWH is consistent with the vascular depression hypothesis from the late-life depression literature. The high rate of functional dependence among PLWH with vascular depression highlights the clinical importance of prospective work on this syndrome in the context of HIV disease.

The effects of carotid revascularization on mood symptoms and quality of life in patients with high - grade carotid stenosis

Carotid occlusive disease has been related to ischaemic strokes and cerebral hypoperfusion, thus affecting patients' quality of life, mainly because of cognitive decline and depressive symptoms. Carotid revascularization techniques [carotid endarterectomy (CEA) and carotid artery stenting (CAS)] may, postoperatively, have a positive impact on patients' quality of life and mental condition, though there have been also presented elusive findings and controversial results. The aim of the present study is to evaluate the effect of carotid revascularization (CEA, CAS) on patients' psychological condition and quality of life through a baseline and follow-up examination. We present data of a group of 35 patients (age range:60-80 years, ΜA=70,26-SD=9,05) with severe, left or right, carotid artery stenosis (>75%), presented with or without symptoms, who underwent surgical treatment with CEA or CAS. Baseline and follow-up (6 months post-surgery) evaluation was conducted in order to assess patients' depressive symptoms and quality of life, through completion of the Beck Depression Inventory and WHOQOL-BREF Inventory, respectively. No statistically significant (p < 0,05) effect of the revascularization process on mood or quality of life assessment could be documented for our patients, regardless of the applied technique (CAS or CEA). Our study supports existing evidence that all of the traditional vascular risk factors represent active participants in the inflammatory process, which has also been implicated in the pathophysiology of depression as well as in pathogenesis of atherosclerotic processes. Thus we have to illuminate new links between the two nosological entities, in the crossroads of psychiatry, neurology and angiology, through the pathways of inflammatory reactions and endothelium dysfunctions. Even though the effects of carotid revascularization on patient's mood and quality of life, are often characterized by opposing results, pathophysiological processes of "vascular depression" and "post stroke depression" remain a promising interdisciplinary medical domain, sharing both scientific and clinical interests between the fields of neurosciences and vascular medicine. Our results, regarding the bilateral connection of depression and carotid artery disease, advocate a most probable causality link between atherosclerotic process and depressive symptoms, rather than justifying a direct association between depressive disorders and carotid stenosis and inferred cerebral blood flow reduction per se.

Augmentation therapy with tandospirone citrate in vascular depression patients with mild cognitive impairment: A prospective randomized clinical trial

Cognitive impairment is a prominent clinical manifestation of vascular depression (VaDep). The current study aimed to assess the efficacy of tandospirone citrate in VaDep cases with mild cognitive impairment (VaDep-MCI) as well as the role of plasma monoamine neurotransmitters during the treatment. In this single-blind, randomized controlled study, 116 participants were randomly assigned to the tandospirone (tandospirone citrate-escitalopram) and control (escitalopram) groups. The primary endpoints were changes in cognitive test scores from baseline to Week 8, including the Rey Auditory Verbal Learning Test (RAVLT), Semantic Verbal Fluency (SVF) test, Trail Making Test (TMT), Digital Span Test (DST) and Clock Drawing Test (CDT) scores. Generalized estimating equation models were used to examine repeated measures. The results showed that compared with the changes in the control group from baseline to Week 8, the tandospirone group showed more significant changes in SVF score at Weeks 4 (p < 0.05) and 8 (p < 0.001), and TMT (B-A) score at Week 8 (p < 0.05). RAVLT, DST and DCT scores were relatively stable in both groups during the study period. Moreover, mediation analysis showed that these results were not mediated by the alleviation of depression symptoms. Partial Spearman correlation analysis showed that only plasma 5-hydroxytryptamine (5-HT) was positively correlated with Hamilton Depression Rating Scale score after Bonferroni correction (r = 0.347, p < 0.001). Augmentation therapy with tandospirone citrate improved the executive and language functions of VaDep-MCI patients. Additionally, plasma 5-HT levels may serve as a potential biomarker of VaDep severity. These findings may provide clinical insights into the treatment of vascular depression.

White matter hyperintensities are an independent predictor of cognitive decline 3 years following first-ever stroke—results from the PROSCIS-B study

BackgroundWhite matter hyperintensities (WMH) are the result of cerebral small vessel disease and may increase the risk of cognitive impairment (CI), recurrent stroke, and depression. We aimed to explore the association between selected cerebrovascular risk factors (CVRF) and WMH load as well as the effect of increased WMH burden on recurrent vascular events, CI, and depression in first-ever ischemic stroke patients.Methods431 from the PROSpective Cohort with Incident Stroke (PROSCIS) were included; Age-Related White Matter Changes (ARWMC) score was used to assess WMH burden on FLAIR. The presence of CVRF (defined via blood pressure, body-mass-index, and serological markers of kidney dysfunction, diabetes mellitus, and hyperlipoproteinemia) was categorized into normal, borderline, and pathological profiles based on commonly used clinical definitions. The primary outcomes included recurrent vascular events (combined endpoint of recurrent stroke, myocardial infarction and/or death), CI 3 years post-stroke, and depression 1-year post-stroke.ResultsThere was no clear association between CVRF profiles and WMH burden. High WMH lesion load (ARWMC score ≥ 10) was found to be associated with CI (adjusted OR 1.05 [95% CI 1.00–1.11]; p < 0.02) in a mixed-model analysis. Kaplan–Meier survival analysis showed a visible increase in the risk of recurrent vascular events following stroke; however, after adjustment, the risk was non-significant (HR 1.5 [95% CI 0.76–3]; p = 0.18). WMH burden was not associated with depression 1-year post stroke (adjusted OR 0.72 [95% CI 0.31–1.64]; p = 0.44).ConclusionHigher WMH burden was associated with a significant decline in cognition 3 years post-stroke in this cohort of first-ever stroke patients.

PC012 / #460 MULTIMODAL EFFECTS OF REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION ON PATIENTS WITH MAJOR DEPRESSION AND VASCULAR DEPRESSION: A PILOT STUDY: E-POSTER VIEWING

The antidepressant potential of repetitive transcranial magnetic stimulation (rTMS) is widely recognized [1], whereas the impact on the neurotrophins involved in major depression (MD) and vascular depression (VD) has not been fully investigated yet [2-3]. We evaluated the effect of rTMS on mood, cognition, neurotrophic factors, motor evoked potentials (MEPs) to TMS, and cerebral blood flow (CBF) to transcranial doppler (TCD) in a pilot series of MD and VD patients.

Involvement of the gut-brain axis in vascular depression via tryptophan metabolism: A benefit of short chain fatty acids

Cerebral hemodynamic dysfunction and hypoperfusion have been found to underlie vascular depression, but whether the gut-brain axis is involved remains unknown. In this study, a rat model of bilateral common carotid artery occlusion (BCCAO) was adopted to mimic chronic cerebral hypoperfusion. A reduced sucrose preference ratio, increased immobility time in the tail suspension test and forced swim test, and compromised gut homeostasis were found. A promoted conversion of tryptophan (Trp) into kynurenine (Kyn) instead of 5-hydroxytryptamine (5-HT) was observed in the hippocampus and gut of BCCAO rats. Meanwhile, 16S ribosomal RNA gene sequencing suggested a compromised profile of the gut SCFA-producing microbiome, with a decreased serum level of SCFAs revealed by targeted metabolomics analysis. With SCFA supplementation, BCCAO rats exhibited ameliorated depressive-like behaviors and improved gut dysbiosis, compared with the salt-matched BCCAO group. Enzyme-linked immunosorbent assays and quantitative RT–PCR suggested that SCFA supplementation suppressed the conversion of Trp to Kyn and rescued the reduction in 5-HT levels in the hippocampus and gut. In addition to inhibiting the upregulation of inflammatory cytokines, SCFA supplementation ameliorated the activated oxidative stress and reduced the number of microglia and the expression of its proinflammatory markers in the hippocampus post BCCAO. In conclusion, our data suggested the participation of the gut-brain axis in vascular depression, shedding light on the neuroprotective potential of treatment with gut-derived SCFAs.

The enigma of vascular depression in old age: a critical update.

Depression is common in older individuals and is associated with high disability and increased mortality, yet the factors predicting late-life depression (LLD) are poorly understood. The relationship between of depressive disorder, age- and disease-related processes have generated pathogenic hypotheses and provided new treatment options. LLD syndrome is often related to a variety of vascular mechanisms, in particular hypertension, cerebral small vessel disease, white matter lesions, subcortical vascular impairment, and other processes (e.g., inflammation, neuroimmune regulatory dysmechanisms, neurodegenerative changes, amyloid accumulation) that may represent etiological factors by affecting frontolimbic and other neuronal networks predisposing to depression. The "vascular depression" hypothesis suggests that cerebrovascular disease (CVD) and vascular risk factors may predispose, induce or perpetuate geriatric depressive disorders. It is based on the presence of various cerebrovascular risk factors in many patients with LLD, its co-morbidity with cerebrovascular lesions, and the frequent development of depression after stroke. Other findings related to vascular depression are atrophy of the medial temporal cortex or generalized cortical atrophy that are usually associated with cognitive impairment. Other pathogenetic hypotheses of LLD, such as metabolic or inflammatory ones, are briefly discussed. Treatment planning should consider there may be a modest response to antidepressants, but several evidence-based and novel treatment options for LLD exist, such as electroconvulsive therapy, transcranial magnetic stimulation, neurobiology-based psychotherapy, as well as antihypertension and antiinflammatory drugs. However, their effectiveness needs further investigation, and new methodologies for prevention and treatment of depression in older individuals should be developed.

Interactions between red and processed meat consumption and APOA5 gene variants associated with the incidence of metabolic syndrome in Korean adults

BackgroundMetabolic syndrome (MetS) is characterized by the coexistence of disorders such as diabetes, hypertension, hyperlipidemia, and obesity and is affected by genetic factors. Previous genome-wide association studies (GWAS) suggested that APOA5 gene variants were significantly associated with MetS and its components. Dietary factors such as red and processed meat consumption can cause chronic diseases, including hypertension, diabetes, and vascular depression. The aim of this study was to investigate the modulation of the incidence of MetS by the interaction between APOA5 rs662799 polymorphism and red and processed meat consumption.MethodsIn this prospective cohort study, 3266 participants were collected from the Korea Association REsource (KARE) cohort of the Korean Genome and Epidemiology Study (KoGES) from 2001 to 2016. APOA5 rs662799 polymorphism was extracted by GWAS using the Korean Chip. Red and processed meat consumption data were assessed using a semi-quantitative food frequency questionnaire.ResultsThe incidence of MetS in carriers of the minor G allele of rs662799 (AG + GG) and the third tertile of red and processed meat consumption (serving/day) was higher than those with the major allele of rs662799 (AA) and the first tertile of red and processed meat consumption (HR 1.70, 95% CI 1.30–2.22, p interaction = 0.002).ConclusionsAn association between the presence of the minor alleles of rs662799 and high red and processed meat consumption and the incidence of MetS was observed in Korean adults.

P150. IN-HOSPITAL COMPLICATIONS IN BREAST RECONSTRUCTION ADMISSION: AN ANALYSIS OF 7438 PATIENTS

PURPOSE: Autologous breast reconstructions are often challenging and these patients sometimes sustain complications during their admission stay. The goal of our study was to assess risk factors for in-hospital complications, morbidity, and mortality in these patients. METHODS: Breast reconstruction patients were admitted and analyzed using the National Inpatient Sample database, 2005-2014. Demographics, clinical data, and outcomes were gathered. The relationships between complications, morbidity, mortality, and the predictors were assessed using a multivariable logistic regression model. RESULTS: 7,438 patients were analyzed. The mean age was 52. The patients were classified based on type of autologous reconstruction: free flap (62.7%) or pedicled flap (37.3%). The mean hospital length of stay (HLOS) was 3.37 days in patients who underwent pedicled flaps and 3.12 days for free flaps. The mean modified frailty index score was significantly higher (0.79) in patients reconstructed with pedicled flaps versus free flaps (0.54). 6.2% of all cases manifested complications which were significantly positively correlated to comorbidities such as obesity, diabetes, hypertension, heart disease, peripheral vascular disease, renal failure, depression, and deficiency anemia. Additionally, the patients with these comorbidities demonstrated higher HLOS, 5.73 vs. 2.98 days (p<0.001) and reoperation rate 1.5% vs. 0.3% (p<0.001). CONCLUSION: Comorbidities were independent predictors of in-hospital complications for patients undergoing autologous breast reconstruction. Patients with these comorbidities manifested higher rates of reoperation and HLOS regardless of the type of autologous reconstruction. Stratifying patients utilizing these comorbidities and the modified frailty index score may be helpful in predicting in-hospital complications for patients undergoing autologous breast reconstruction.

Treatment response in late-life depression: the absence of a relationship with white matter hyperintensity volume, executive functioning, and processing speed

Treatment response in late-life depression: the absence of a relationship with white matter hyperintensity volume, executive functioning, and processing speed

Postoperative Delirium in Lung Cancer Anatomical Resection-Analysis of Risk Factors and Prognosis.

The incidence of postoperative delirium after anatomical lung resection ranges from 5 to 16%. This study aimed to analyze the risk factors and prognosis of postoperative delirium in anatomical lung resection for lung cancer. This study included 1351 patients undergoing anatomical lung resection between April 2010 and October 2020. We analyzed the perioperative risk factors of postoperative delirium. We also compared postoperative complications and survival between the delirium and non-delirium groups. Postoperative delirium was identified in 44 (3.3%) of 1351 patients who underwent anatomical lung resection for lung cancer. Age, peripheral vascular disease, depression, and current smoking status were independent risk factors for postoperative delirium in the multivariate analysis. The percentage of postoperative delirium was 0.6% in never smokers and 6.0% in current smokers. The delirium and non-delirium groups showed significant differences in overall survival (p = 0.0144) and non-disease-specific survival (p = 0.0080). After propensity score matching, the two groups did not significantly differ in overall survival (p = 0.9136), non-disease-specific survival (p = 0.8146), or disease-specific survival (p = 0.6804). Age, peripheral vascular disease, depression, and current smoking status were considered independent risk factors for postoperative delirium in anatomical lung resection for lung cancer. Smoking cessation for at least four weeks before surgery is recommended for reducing incidence of post-operative delirium.

The relationship of carotid artery disease with mental and neurocognitive disorders

Carotid stenosis constitutes a common vascular disease that significantly affects cerebral blood flow and thus is associated with patients' cognitive functions. Carotid revascularization techniques [carotid endarterectomy (CEA) and carotid artery stenting (CAS)] may benefit cognition, though there are opposing findings, reporting an apparent decrement in cognitive function, no effect, or an apparent improvement after revascularization. A great number of studies are trying to evaluate the effect of carotid revascularization (CEA, CAS) on patients' cognitive functions, as well as on their psychological condition and quality of life through a baseline and follow-up neuropsychological examination. Recent reviews refer only to the narrow limits of cognitive deficits that may be attributed to carotid stenosis, rather than elucidating the outfit of all aspects of mental and cognitive correlations. Most of those findings depict controversy in current literature as far as the neuropsychological effects of carotid revascularization techniques are concerned, while clinical entities of "vascular dementia" and "vascular depression", as well as intercurrent vascular risk factors are also addressed. This might be taken into consideration, when determining the optimal therapeutic strategy for tackling carotid artery occlusive disease, while best practice clinical decisions should be still focused on stroke prevention and symptoms alleviation, until further research on the field of neuroangiology presents undisputable conclusions regarding the underlying effects of revascularization on mood and cognition. Τhe neurovascular interface, as far as mental and neurocognitive impact of carotid stenosis is concerned, also, comprises, the conceptual pathophysiological entity of "atheroinflammation", underscoring the association of vascular lesions with cognitive impairment, major depressive disorder and bipolar disorder. Chronic recurrent ischemia and chronic low perfusion are also addressed from neurocognitive aspect, regarding therapeutic strategies that might be preferred so as to reduce the burden of chronic cerebrovascular disease in both symptomatic and asymptomatic patients, given the fact that inflammatory processes of vascular complexion underlie both neuroinflammation and atherosclerosis, affecting cerebral perfusion as well as cortical blood flow.

Transnosographic analysis of executive dysfunction – clinical, psychometric and therapeutic dimensions

The analysis of executive dysfunction in patients with mental disorders presents clinical and therapeutic importance, based on research that supports the involvement of this component in shaping the symptomatic picture and in determining the recovery prognosis. Although therapeutic approaches that specifically target cognitive impairments (in schizophrenia, vascular depression, ADHD etc.) are not yet used on a large scale, they can be considered augmentation strategies with the potential to improve the patients’ recovery and quality of life. A structured assessment of the executive functioning in clinical setting, using validated psychometric methods, is recommended in order to monitor as completely as possible the patients’ mental status and the adaptive difficulties generated by these cognitive problems. The current analysis will include aspects related to the correlations between executive dysfunction and specific psychiatric symptoms, on the one hand, as well as psychosocial functioning, on the other hand. The study of endophenotypes, which occupy an intermediate position between genotypes and clinical manifestations (phenotypes), can help reduce the heterogeneity of some nosographic categories and can motivate early therapeutic intervention strategies. Another dimension of the present analysis refers to the impact of specific therapies, pharmacological, psychosocial or neurostimulation, on executive dysfunction. This first part of the review presents data on executive dysfunction in schizophrenia, major depressive disorder, vascular depression, bipolar disorder, neurocognitive disorders and eating disorders.

Secular trends in prevalent mild cognitive impairment: Data from the Swedish population-based study Good Aging in Skåne.

BackgroundResearch suggests that incident dementia is decreasing, yet research on secular trends of prodromal dementia such as mild cognitive impairment (MCI) is lacking.MethodsTo determine change of MCI prevalence over time and potential explanatory factors, four baseline samples (years 2001–2020) of Swedish participants (n = 3910) aged 60 and 81 at examination were compared.ResultsAn overall drop of 9 to 10 percentage points in MCI prevalence between 2001 and 2020 was observed, with lower odds ratios (OR) for MCI in the latest birth cohorts compared to earliest (e.g., ORs for 60‐year‐olds in latest born = 0.53; 95% confidence interval [CI] 0.37–0.76). Adjustments for sociodemographic (e.g., education), lifestyle, vascular and metabolic health and depression could not fully explain the observed MCI decline (e.g., 60‐year‐olds, OR = 0.59; 95% CI 0.40–0.88).DiscussionStudies like this are imperative as even a slight postponement in the onset of dementia could have a substantial impact on future public health burden.

Pathomechanisms of Vascular Depression in Older Adults.

Depression in older individuals is a common complex mood disorder with high comorbidity of both psychiatric and physical diseases, associated with high disability, cognitive decline, and increased mortality The factors predicting the risk of late-life depression (LLD) are incompletely understood. The reciprocal relationship of depressive disorder and age- and disease-related processes has generated pathogenic hypotheses and provided various treatment options. The heterogeneity of depression complicates research into the underlying pathogenic cascade, and factors involved in LLD considerably differ from those involved in early life depression. Evidence suggests that a variety of vascular mechanisms, in particular cerebral small vessel disease, generalized microvascular, and endothelial dysfunction, as well as metabolic risk factors, including diabetes, and inflammation that may induce subcortical white and gray matter lesions by compromising fronto–limbic and other important neuronal networks, may contribute to the development of LLD. The “vascular depression” hypothesis postulates that cerebrovascular disease or vascular risk factors can predispose, precipitate, and perpetuate geriatric depression syndromes, based on their comorbidity with cerebrovascular lesions and the frequent development of depression after stroke. Vascular burden is associated with cognitive deficits and a specific form of LLD, vascular depression, which is marked by decreased white matter integrity, executive dysfunction, functional disability, and poorer response to antidepressive therapy than major depressive disorder without vascular risk factors. Other pathogenic factors of LLD, such as neurodegeneration or neuroimmune regulatory dysmechanisms, are briefly discussed. Treatment planning should consider a modest response of LLD to antidepressants, while vascular and metabolic factors may provide promising targets for its successful prevention and treatment. However, their effectiveness needs further investigation, and intervention studies are needed to assess which interventions are appropriate and effective in clinical practice.